The hypothesis is that angiotensin-II (A-II) diminishes insulin's suppression of lipolysis, increasing the flux of fatty acid into cholesterol pathways, and linking these factors to atherosclerosis. Preliminary data using the euglycemic clamp and stable isotope methods show decreased insulin suppression of lipolysis when A-II is infused. In support of the hypothesis, enalapril (which decreases A-II) improved insulin-mediated lipolysis suppression in the hypertensive (insulin-resistant) subject.